Feeling what you hear: auditory signals can modulate tactile tap perception

We tested whether auditory sequences of beeps can modulate the tactile perception of sequences of taps (two to four taps per sequence) delivered to the index fingertip. In the first experiment, the auditory and tactile sequences were presented simultaneously. The number of beeps delivered in the auditory sequence were either the same as, less than, or more than the number of taps of the simultaneously presented tactile sequence. Though task-irrelevant (subjects were instructed to focus on the tactile stimuli), the auditory stimuli systematically modulated subjects tactile perception; in other words subjects responses depended significantly on the number of delivered beeps. Such modulation only occurred when the auditory and tactile stimuli were similar enough. In the second experiment, we tested whether the automatic auditory-tactile integration depends on simultaneity or whether a bias can be evoked when the auditory and tactile sequence are presented in temporal asynchrony. Audition significantly modulated tactile perception when the stimuli were presented simultaneously but this effect gradually disappeared when a temporal asynchrony was introduced between auditory and tactile stimuli. These results show that when provided with auditory and tactile sensory signals that are likely to be generated by the same stimulus, the central nervous system (CNS) tends to automatically integrate these signals.     

A recent polyploidy superimposed on older large-scale duplications in the Arabidopsis genome

The Arabidopsis genome contains numerous large duplicated chromosomal segments, but the different approaches used in previous analyses led to different interpretations regarding the number and timing of ancestral large-scale duplication events. Here, using more appropriate methodology and a more recent version of the genome sequence annotation, we investigate the scale and timing of segmental duplications in Arabidopsis. We used protein sequence similarity searches to detect duplicated blocks in the genome, used the level of synonymous substitution between duplicated genes to estimate the relative ages of the blocks containing them, and analyzed the degree of overlap between adjacent duplicated blocks. We conclude that the Arabidopsis lineage underwent at least two distinct episodes of duplication. One was a polyploidy that occurred much more recently than estimated previously, before the Arabidopsis/Brassica rapa split and probably during the early emergence of the crucifer family (24-40 Mya). An older set of duplicated blocks was formed after the monocot/dicot divergence, and the relatively low level of overlap among these blocks indicates that at least some of them are remnants of a larger duplication such as a polyploidy or aneuploidy.     

Eimeria tenella microneme protein EtMIC3: identification, localisation and role in host cell infection

The gene coding for Eimeria tenella protein EtMIC3 was cloned by screening a sporozoite cDNA library with two independent monoclonal antibodies raised against the oocyst stage. The deduced sequence of EtMIC3 is 988 amino acids long. The protein presents seven repeats in tandem, with four highly conserved internal repeats and three more divergent external repeats. Each repeat is characterised by a tyrosine kinase phosphorylation site, WRCY, and a reminiscent motif of the thrombospondin1 (TSP1)-type I domain, CXXXCG. The protein EtMIC3 is localised at the apex of free parasite stages. It is not detected in the early intracellular parasite stage but is synthesised in mature schizonts. Secretion of the protein is induced when sporozoites are incubated in complete medium at 41 degrees C. Strangely enough, the two independent mAb that allow cloning of EtMIC3 interfere with parasitic growth in different ways. One is able to inhibit parasite invasion whereas the other inhibits development. Expression and localisation of the protein EtMIC3 are consistent with a protein involved in the invasion process as is expected for a microneme protein.     

Corticoliberin, somatocrinin and amine contents in normal and parkinsonian human hypothalamus

We have compared hypothalamic contents of various neurotransmitters (dopamine (DA), norepinephrine and serotonin) and their metabolites (dihydroxyphenyl acetic acid, homovanilic acid, 5-hydroxyindoleacetic acid) in post-mortem human controls and parkinsonian hypothalami. Neurotransmitters and their metabolites were measured in 0.1 N HCl hypothalami extracts using electrochemical detection after high performance liquid chromatography. Using specific radioimmunoassays we have also measured corticoliberin and somatocrinin contents in these hypothalami. Despite a 50% decrease of DA contents in parkinsonian hypothalami, no variations of corticoliberin and somatocrinin contents were found: 16.6 +/- 1.78 pg/mg tissue in Parkinson disease vs 16.71 +/- 1.89 in controls for human corticotropin-releasing factor (hCRF 1-41) and 37.38 +/- 11 vs 45.16 for human growth-hormone-releasing factor (hGRF 1-44).     

Monitoring of basophil activation using CD63 and CCR3 in allergy to muscle relaxant drugs

Allergic or pseudoallergic reactions that occur during anesthesia have been increasing for the last few years. To date, the diagnosis of allergy to muscle relaxants remains difficult. In this respect, we developed a flow cytometric method for the study of drug-induced basophil degranulation using CD63 and CCR3. Fifty patients who developed clinical features evocative of allergic reactions immediately after induction of anesthesia were included and classified into two groups. Group 1 (n = 39) comprised true allergic patients, who developed typical signs of shock associated to positive skin testing. Group 2 (n = 11) consisted of patients whose clinical history was not typical and skin testing was negative or nonconclusive. Seventeen control subjects were also studied in this report. We compared data from flow cytometry to skin tests, specific IgE, and histamine release results. Flow cytometry showed a sensitivity of 54%, while that of specific IgE was similar, at 62%. Interestingly, when considering the sensitivity of IgE + CD63 for diagnosis, we reached a sensitivity value of 80%. Of 15 negative results for specific IgE, we found 7 positive CD63 tests, while histamine release gave positive results in only 2 cases. Furthermore, the CD63 protocol showed good specificity (100%). We conclude that our flow cytometry protocol is a promising tool in allergy diagnosis since it is specific and complementary to specific IgE detection.     

Chronology of the push pull effect on nonhuman primates—shift of the arterial pressure threshold

Fighter pilots are frequently exposed to high Gz acceleration which may induce in-flight loss of consciousness (G-LOC). One factor reducing tolerance to accelerations is a previous exposure to negative accelerations. This phenomenon, which happens during the first few seconds after the onset of the positive plateau, is called the push pull effect. Our goal was to validate a non human primate model in order to study push pull physiological mechanisms and possible changes in arterial pressure, which may occur after the first ten seconds of the positive acceleration plateau. Eight rhesus monkeys were centrifuged in profile runs, including positive Gz accelerations (+1.4, +2 and +3 Gz) with or without previous negative Gz acceleration (–2 and –3 Gz vs. +1.4 Gz). Heart rate, blood pressure and esophageal pressure were recorded during the entire centrifugation run. Results showed that the push pull effect was observed in the non human primate model. Moreover, the reduced tolerance to acceleration lingered longer than that during the first ten seconds after exposure to +Gz acceleration. It was found that, after the fourteenth second, mean blood arterial pressure stabilizes at a lower value, when the positive acceleration is preceded by a negative acceleration (15.8 kPa for –1 Gz and 15.5 for –2 Gz vs. 16.9 for 1.4 Gz). The chronology of the push pull effect seems to involve two periods. One has a short time span. The other one has a longer time span and could be induced by shift of pressure threshold, coming from exposure to previous negative acceleration.     

Gastric myeloid metaplasia: a case report and review of the literature

We report a case of gastric myeloid metaplasia in an 89- year-old woman with agnogenic myeloid metaplasia. The lesions were fortuitously discovered on upper endoscopy. The antral mucosa was thickened and polypoid, and on histologic examination contained immature granulocytes, megakaryocytes, and a few erythroblasts without desmoplastic stromal reaction. The granulocytes were positive for CD15, CD68, and myeloperoxidase on immunohistochemistry, and the megakaryocytes showed positive reactivity for factor VIII. Gastric myeloid metaplasia is a very rare event, and to our knowledge only 6 cases have been reported in the literature to date. It usually occurs in patients with advanced myeloproliferative syndrome. Gastric myeloid metaplasia often has a pseudotumoral appearance, leading to digestive symptoms. Histologic diagnosis is straightforward when trilinear hematopoietic elements are identified in gastric biopsies. Immunohistochemistry with anti-factor VIII antibody can be useful to confirm the presence of megakaryocytes.     

Dysferlin mutations in LGMD2B, Miyoshi myopathy, and atypical dysferlinopathies

DYSF encoding dysferlin is mutated in Miyoshi myopathy and Limb-Girdle Muscular Dystrophy type 2B, the two main phenotypes recognized in dysferlinopathies. Dysferlin deficiency in muscle is the most relevant feature for the diagnosis of dysferlinopathy and prompts the search for mutations in DYSF. DYSF, located on chromosome 2p13, contains 55 coding exons and spans 150 kb of genomic DNA. We performed a genomic analysis of the DYSF coding sequence in 34 unrelated patients from various ethnic origins. All patients showed an absence or drastic decrease of dysferlin expression in muscle. A primary screening of DYSF using SSCP or dHPLC of PCR products of each of 55 exons of the gene was followed by sequencing whenever a sequence variation was detected. All together, 54 sequence variations were identified in DYSF, 50 of which predicting either a truncated protein or one amino-acid substitution and most of them (34 out of 54) being novel. In 23 patients, we identified two pathogenic mutations, while only one was identified in 11 patients. These mutations were widely spread in the coding sequence of the gene without any mutational "hotspot."